Muramatsu Y, Yamada T, Moralejo D H, Suzuki Y, Matsumoto K
Institute for Animal Experimentation, University of Tokushima School of Medicine, Japan.
Res Commun Mol Pathol Pharmacol. 1998 Sep;101(3):225-31.
LEC rats are defective at the p-type copper transport ATPase gene (Atp7b) and exhibit excessive hepatic copper accumulation. However, copper concentration in fetal liver of LEC rats is lower than that of F344 normal rats. In this study, we made fetal backcrosses between LEC and F344 normal rats. At 19 days of gestation, hepatic copper concentrations of (LECXF344)F1XLEC and LECX(LECXF344)F1 fetuses were equivalent to those of F344 and LEC fetuses, respectively, irrespective of their Atp7b genotype. Furthermore, Atp7b expression was identified in the uterus and the maternal portion of placenta, but not in the fetal portion of placenta, in pregnant F344 rats. From these results, we speculate that the Atp7b product might contribute to a copper transport system from mother to fetus in the maternal portion, but not in the fetal portion of placenta.